腦是人體對(duì)缺氧最為敏感的器官，腦組織缺血將會(huì)導(dǎo)致局部腦組織及其功能的損害,，遭受一定時(shí)間缺血的組織細(xì)胞恢復(fù)血流（再灌注）后也可造成腦功能嚴(yán)重受損,而組織損傷程度迅速劇增的情況稱缺血再灌注損傷,。近年來(lái)，關(guān)于腦缺血再灌注損傷與血腦屏障破壞的研究已成為一個(gè)重要內(nèi)容,。
一項(xiàng)關(guān)于“Rho kinase: a new target for treatment of cerebral ischemia/reperfusion injury”的研究表明,，鹽酸法舒地爾可明顯促進(jìn)腦缺血再灌注后神經(jīng)功能恢復(fù)，改善血腦屏障功能,，明顯抑制RhoA蛋白表達(dá),，上調(diào)生長(zhǎng)相關(guān)蛋白-43和Claudin-5蛋白表達(dá)。作者認(rèn)為,，針對(duì)Rho激酶進(jìn)行干預(yù)可能是腦缺血再灌注治療的一個(gè)新靶點(diǎn),。此項(xiàng)研究發(fā)表在2013年5月第13期的《中國(guó)神經(jīng)再生研究（英文版）》雜志中。（生物谷 Bioon.com）
生物谷推薦的英文摘要
Neural Regeneration Research DOI：10.3969/j.issn.1673-5374.2013.13.003
Rho kinase A new target for treatment of cerebral ischemia/reperfusion injury
Qinghong Cui, Yongbo Zhang, Hui Chen, Jimei Li
Rho kinase inhibitor fasudil hydrochloride has been shown to reduce cerebral vasospasm, to inhibit inflammation and apoptosis and to promote the recovery of neurological function. However, the effect of fasudil hydrochloride on claudin-5 protein expression has not been reported after cerebral ischemia/reperfusion. Therefore, this study sought to explore the effects of fasudil hydrochloride on blood-brain barrier permeability, growth-associated protein-43 and claudin-5 protein expression, and to further understand the neuroprotective effect of fasudil hydrochloride. A focal cerebral ischemia/reperfusion model was established using the intraluminal suture technique. Fasudil hydrochloride (15 mg/kg) was intraperitoneally injected once a day. Neurological deficit was evaluated using Longa’s method. Changes in permeability of blood-brain barrier were measured using Evans blue. Changes in RhoA, growth-associated protein-43 and claudin-5 protein expression were detected using immunohistochemistry and western blotting. Results revealed that fasudil hydrochloride noticeably contributed to the recovery of neurological function, improved the function of blood-brain barrier, inhibited RhoA protein expression, and upregulated growth-associated protein-43 and claudin-5 protein expression following cerebral ischemia/reperfusion. Results indicated that Rho kinase exhibits a certain effect on neurovascular damage following cerebral ischemia/reperfusion. Intervention targeted Rho kinase might be a new therapeutic target in the treatment of cerebral ischemia/reperfusion.
